Cancer-Fighting Abilities of Sorghum and Foxtail Millet Compounds

Cancer-Fighting Abilities of Sorghum and Foxtail Millet Compounds

Cancer-Fighting Abilities of Sorghum and Foxtail Millet Compounds

 

Breast and prostate cancers are leading causes of global cancer mortality, typically managed through a combination of medication and dietary adjustments. Recent research at Dr. Ambedkar Institute of Technology has focused on phytochemicals extracted from Sorghum bicolor and Setaria italica, targeting Dihydrofolate reductase (DHFR) to hinder cancer cell proliferation.

In a comprehensive literature survey, the study identified 50 phytochemicals from Sorghum and Foxtail millets. Utilizing molecular docking, the research assessed their binding affinity with DHFR, revealing robust stability within DHFR's active site for compounds like caffeic acid, ferulic acid, hesperetic acid, stigmasterol, Cis-p-Coumaric acid, and luteolinidin (docking scores: -5.4 to -6.7 kcal/mol). These scores were comparable to standard drugs such as flutamide and capecitabine (-7.5 and -8.1 kcal/mol, respectively).

Moreover, using density functional theory (DFT), the study verified these phytochemicals' stable interactions with DHFR, bolstering their potential as effective inhibitors. This research extends prior work focusing on growth factor receptors (GFRs) in cancer cells, now emphasizing DHFR's pivotal role in hindering cell growth through millet-derived phytochemicals.Given the substantial global cancer burden—18.1 million new cases and 9.6 million deaths in 2018—integrating millet grains into diets alongside conventional treatments could potentially reduce incidence and mortality rates of breast and prostate cancers. Dr. Ambedkar Institute's findings propose millet-derived phytochemicals as promising DHFR inhibitors, warranting further validation through in vivo and clinical studies.

In conclusion, Dr. Ambedkar Institute of Technology's research underscores Sorghum and Foxtail millet-derived phytochemicals as promising candidates for inhibiting DHFR in breast and prostate cancer management. This conclusion is supported by comprehensive molecular docking, DFT calculations, and pharmacokinetic analyses.

 


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